In a study published in 1995 in the American Journal of Kidney Diseases, Dolson et al demonstrated that a rapid decrease of serum potassium concentrations during haemodialysis would produce a significant increase in systolic blood pressure at the end of the session, even though there were no clear effects on intra-dialytic blood pressure. The authors defined this post-dialysis blood pressure behaviour as "rebound hypertension". Paradoxically, in animal models, other than in the context of end-stage renal disease, potassium is a vasodilator. Considering that the removal of potassium during the haemodialysis session could be theoretically modulated in profiles (as with sodium and bicarbonate), it was deemed suitable to delve deeper into this argument by studying, in detail, the (non invasive) hemodynamic repercussions of changes in the potassium concentration of the dialysate. Not being able to linearly modify the concentration, we decided to divide the dialysis session in 3 tertiles, randomising the patients to all possible dialysate sequences containing the usual concentration of potassium or two cut-off points at +1 and -1 mmol/l. Haemodynamic measurements were performed using a finger beat-to-beat monitor.